OK, and how do you know that this transposition was the result of a mistaken in replication rather than a sequence that was already there?
I know this is a radical idea for you so brace yourself - why not read some of the papers on it? That way you might at least know what it is you're objecting too.
Here's a bit of a commentary that might help.
quote:These are the salient results of the vanâ€™t Hoff et al paper:
The gene where the change resides that made the light-colored moths dark is called cortex, and is known in Drosophila to be involved in cell division of the egg in females. It wasnâ€™t known, at least in flies, to be involved in color.
The association between cortex and color was found by â€œassociation mappingâ€ in B. betularia. The researchers took a bunch of moths of both the carbonaria and typica forms (and insularia as well), and sequenced DNA in the region where the mutation was known to reside, looking for a consistent change in the DNA that would distinguish the various forms with near-perfect ability.
The change was found not to be a single-base mutation in the DNA, but an insertion of a â€œtransposable elementâ€ (or â€œtransposonâ€)â€”a bit of DNA that can move around in the genomeâ€”into the carbonaria form. The whole inserted region comprises 21,925 nucleotides, and involves a single element present in 2.3 copies that has moved as a unit into the cortex gene.
The transposable element actually activated (rather than silenced) the cortex gene, increasing the amount of its product in a manner we donâ€™t understand. Curiously, the increased gene activity in the dark form was far more pronounced in larvae (caterpillars, which the paper calls â€œcrawlersâ€) rather than pupae or adults, presumably because the precursors for scale development and their color are being formed at this stage of development.
The association between the transposon and color was nearly perfect, but not 100% so. Every one of the typica and insularia moths lacked the element, while 105 of 110 black carbonaria forms had the element. This means that other genes besides cortex may influence colorâ€”or developmental/environmental effects that arenâ€™t geneticâ€”but that the insertion in cortex is likely the most important one: the one that produced the fuel for natural selection on color.
By looking at the DNA around the transposon, the researchers could estimate the age of the mutation. If it arose recently in a single individual, most carriers of the mutation would have similar sequences nearby, as recombination wouldnâ€™t have time to put the transposon next to varied DNA from other individuals. If the mutation was old, the surrounding regions of the carbonaria form would be more diverse, as recombination would have combined the inserted gene with other nearby genes from different individuals. Using simulations, the researchers gave the most likely date of the mutation as 1819, shortly before it was first seen in the wild. The â€œinterquartile rangeâ€ for the dates, which I take to be the range of dates between the 25% and 75% likelihood that it originated, is 1681-1806. Below is the graph showing the probability density of when the mutation to carbonaria originated (i.e., when the transposon moved). You can see that all the dates are fairly recent, so this mutation did not occur thousands of years ago. The highest probability is at 1819, not far from when it was first seen in the wild (1848; dotted line). A new variant butterfly would be found pretty quickly by the Brits, who are avid butterfly and moth collectors!
You might also note this regarding your other problem:
quote:The mutation occurred only shortly before the environmental changeâ€”pollutionâ€”that caused the evolution of the color difference. Thatâ€™s interesting, but it wasnâ€™t necessary, for mutations like this occur continuously, and can hang around permanently. Thatâ€™s because, although natural selection weeds such genes out of populations (dark moths would be at a disadvantage before the Industrial Revolution), mutation keeps putting them back in, so there is a reservoir of low-frequency mutations hanging around that could be the basis for a new adaptation should the environment change. (This is called a â€œmutation/selection equilibrium.â€) Remember, though, that those mutations arenâ€™t hanging around for the purpose of providing future adaptive evolution. Errors in DNA happen randomly, cannot arise to anticipate the organismsâ€™s future needs, and sometimes, but not usually, turn out to be useful.
What I "expect" isn't about my own guesses, it's about what I've picked up from YOU GUYS by reading various web sites and so on.
That's a bit strange since I have stated over and over that random mutations can produce beneficial mutations. Obviously, you are ignoring what we are saying.
Where I used to think a single trait such as eye color was probably governed by many genes, it seems now that it's governed by different regions of a single gene?????? How that works I don't yet grasp since I thought a whole gene made a particular protein, which protein is what brought about the trait.
There are multiple genes that can affect eye color, but most variation in eye color is affected by two genes. One of those genes is for the protein, and different mutations will affect the function of that protein. The other gene controls how much of that protein is made.
MC1R is a very famous gene, since it's effect on coloration makes its mutations obvious, and since variation in MC1R plays a role in some of the most immediately obvious variation amongst humans. For the same reasons of obvious phenotypic effect, MC1R has been extensively studied in other animals. Wild boar, for example, are monotypic for MC1R - all wild animals have the same allele. Domestic pigs, however, have at least four different MC1R alleles, which contribute to the huge variation in colour of domestic breeds. Now, it is of course possible that the ancestral wild population contained all these alleles, which have coincidentally been lost by drift in the reduced wild population. It seems much more likely to me, though, that these are all post-domestication mutations which have spread once pigs were removed from the selective constraints of camouflage. This sort of thing has presumably created the canvas from which breeders have selected in many domesticated species.
You may have seen me references this paper before, but there is a great study on MC1R and natural selection in rock pocket mice:
And since you note that there are recognizable differences between chimp and human organs and bones although we have the same organs and bones, evolution has the task of making all those "small" changes in all those parts of the body. Seems to me that's a case of the usual wishful thinking that fuels all the assumptions of the ToE.
As I have already shown, we have the evidence that evolution was responsible for the differences between the chimp and human genomes. It isn't an assumption. The fingerprint of random mutations is all over those genomes.
Every time you say it is an assumption it is a lie. We have the evidence.
Then you need to explain why changes to a genome can never be beneficial. If this were the case then even God could not create different species since any differences from this one and only possible functional genome would be either neutral or detrimental.
Seems to me both the peppered moths and the pocket mice used to be described in more drastic terms: it threatens their very existence if they don't get the other color to save them.
"Used to be described"? Where? I bet you can't cite a single example.
Anyway, the way both situations are being described now there never was really any controversy. So I guess I got it wrong. Both colors were always available and the protective color proliferated when the background made it necessary since the predators would pick off the contrasting color. No controversy after all, nothing interesting really.
The peppered moths were doing just fine in areas where coal ash had not darkened trees and rocks. They didn't need the mutation to survive. The mutation that produced the darker color just allowed them to expand their range into areas where coal ash had darkened the environment. If that mutation had not happened there would have been millions and millions of peppered moths out in the countryside and in other areas around the globe. Wikipedia is your friend:
quote: Biston betularia [the peppered moth] is found in China (Heilongjiang, Jilin, Inner Mongolia, Beijing, Hebei, Shanxi, Shandong, Henan, Shaanxi, Ningxia, Gansu, Qinghai, Xinjiang, Fujian, Sichuan, Yunnan, Tibet), Russia, Mongolia, Japan, North Korea, South Korea, Nepal, Kazakhstan, Kirghizstan, Turkmenistan, Georgia, Azerbaijan, Armenia, Europe and North America.
The pocket mice were doing just with light brown fur that camouflaged them in the light brown desert. The mutation that gave them black fur allowed them to expand their range into areas with black rocks. If that mutation never happened there would still be millions and millions of light brown pocket mice out in the deserts of the southwest US.